Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe a 67-year-old man in who serum KL-6 levels were measured during drug-induced pneumonia. The patient was hospitalized, because of coughing, fever, and dyspnea on exertion after administration of Sho-saiko-to (herbal medicine). After he was hospitalized, his symptoms were relieved, and the infiltration shadow on chest X-ray films resolved, but after re-administration of Sho-saiko-to, fever and hypoxemia developed. The serum KL-6 level was again high one day after oral re-administration of the drug. However, the level of lactate dehydrogenase in serum was not high after the re-administration. After treatment with on oral steroid drug the serum KL-6 level decreased gradually, symptoms were relieved the previously high level of c-reactive protein in serum decreased, the previously high white blood cell count decreased, and radiographic findings returned to normal. The diagnosis of drug-induced pneumonia is difficult, because specific diagnostic measures have not been developed. In the present case the serum KL-6 level increased rapidly after re-administration of the drug, and therefore measurement of serum KL-6 level may be helpful in the diagnosis of drug-induced pneumonia.
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PMID:[Levels of serum KL-6 in a patient with drug-induced pneumonitis]. 934 Dec 89

Eighteen cases of pneumonia developed during an outbreak of adenovirus infection in a chronic psychiatric care facility. The six patients most severely affected were admitted to the intensive care unit (ICU) at our institution. Four of these patients developed septic shock. We report the presentation, disease progression, and response to treatment of these patients. Clinical features consisted of high fever, nonproductive cough, and dense lower lobe infiltrates. Laboratory abnormalities included transient fall in white blood cell and platelet counts, and elevations of transaminases, lactate dehydrogenase (LDH), and creatinine phosphokinase (CPK). Five patients were intubated for hypoxemia and four developed the acute respiratory distress syndrome (ARDS) and septic shock (mean cardiac output, 14.1 +/- 1.3 L/min; cardiac index, 6.4 +/- 0.4 L/min/min2; systemic vascular resistance, 326 +/- 107 dyne cm/s2). All patients recovered and were discharged back to the chronic care facility except for one patient with chronic renal failure who died 2 mo after admission. Adenovirus (serotype 35) was isolated from the respiratory secretions of five patients and antibody titers increased 6-fold in the other. These patients constitute the largest series of patients with ARDS and septic shock caused by adenovirus pneumonia and the first outbreak of multiple cases of adenovirus pneumonia in immunocompetent civilian adults occurring from a single source.
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PMID:Multiple cases of life-threatening adenovirus pneumonia in a mental health care center. 947 84

Inhaled beryllium (Be) can induce a range of adverse pulmonary responses in animals and humans including acute pneumonitis, chronic granulomatous lung disease, and cancer. To facilitate comparisons with our previous data describing Be toxicity in rats, we evaluated the toxic effects of inhaled Be metal in mice. Groups of 34 strain C3H/HeJ mice were acutely exposed by the nose-only route to aerosolized Be metal to achieve measured initial lung burdens of 0, 1.7, 2.6, 12, or 34 microg. All mice received aerosolized 85 Sr-labeled fused aluminosilicate particles (85 Sr-FAPs) immediately before their Be exposure so that the influence of Be on lung retention of these poorly soluble tracer particles could be externally quantitated. Groups of mice were euthanized at 8, 15, 40, 90, 210, and 350 days after exposure for evaluation of histopathological changes and for cytologic and biochemical indicators of lung damage measured in bronchoalveolar lavage fluid. Clearance of 85 Sr-FAP tracer particles through 196 days after exposure was delayed in mice receiving the 12 and 34 microg Be lung burdens, but not the 1.7 or 2.6 microg lung burdens. Increased total cell numbers, increased percentage of neutrophils, and elevated levels of total protein and the activities of beta-glucuronidase and lactate dehydrogenase in bronchoalveolar lavage fluid were observed in the two highest Be lung burden groups compared with controls. Lung lesions included particle-containing macrophages, granulomatous pneumonia, lymphocytic interstitial aggregates, and mononuclear interstitial infiltrates. These lesions were occasionally seen in mice receiving the 2.6 microg lung burden, were present in most of the mice receiving 12 or 34 microg lung burdens, and were generally increased in severity with time and lung burden. Thus, we have demonstrated that a single, acute inhalation exposure to Be metal can chronically retard particle clearance and induce lung damage in mice. The initial lung burdens used caused responses ranging from no apparent effects to significant Be-induced responses. A comparison of these data with our previous data from rats indicates that the mass of Be metal required to induce lung damage in mice is similar to that needed for rats. When expressed on a lung weight-normalized basis, mice appeared to be more resistant to the toxic effects of inhaled Be than rats.
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PMID:Dose-response relationships between inhaled beryllium metal and lung toxicity in C3H mice. 953 46

Fibreoptic bronchoscopy is an established diagnostic procedure for HIV-associated pulmonary infections. We retrospectively evaluated the diagnostic effectivity and safety of fibreoptic bronchoscopy with bronchoalveolar lavage (BAL) and transbronchial biopsy (TBB) in 153 patients with late-stage HIV infection and clinical signs of pulmonary infection or abnormal chest radiograph. Bronchoscopy leads to diagnosis in 82.4% and changed therapy in 54%. 45 patients (30%) were found to have pneumocystis carinii pneumonia (PCP), the most common bronchoscopic finding, followed by bacterial lung disease (29.3%). BAL had a sensitivity of 78% for PCP. Diagnostic yield of BAL for PCP was higher in patients without previous treatment (positive results in 82%) with regard to PCP independend of the prior treatment. Serious complication occurred in 22 cases (pneumothorax: 6 (3.9%), bleeding: 12 (7.8%), hypoxaemia: 4 (2.6%)). High serum levels of lactate dehydrogenase (LDH) correlated with pulmonary complications like pneumothorax. Age, sex and kind of pulmonary infection did not influence complication rates. 6 (3.9%) episodes of spontaneous pneumothorax occurred in the further course, 3 of them concurrently with PCP or prior history of PCP. We conclude that fibreoptic bronchoscopy is of great value for diagnosing pulmonary infection in HIV-seropositive patients. TBB provides incremental diagnostic information not available from BAL, especially in patients pretreated with cotrimoxazol or pentamidin. For that reason we believe that TBB should be performed in these patients.
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PMID:[Results and complications of fiber bronchoscopy in HIV positive patients]. 1002 41

The diagnosis of ventilator-associated pneumonia (VAP) is difficult for several reasons. Firstly, clinical markers show a large percentage of false-positive and false-negative results. Secondly, microbiological diagnosis based on quantitative cultures of protected specimen brush (PSB), bronchoalveolar lavage (BAL), and endotracheal aspirates also present false-positive and false-negative results. Furthermore, definite results are delayed for 48-72 hours. For all these reasons it would be an advantage to have a biological marker of ventilator-associated pneumonia in clinical practice. Since clinical features of pneumonia in mechanically ventilated patients are neither specific nor sensitive, rapid markers of pneumonia might be of great assistance to the clinician in deciding whether to start an empiric antibiotic regimen. A marker of ventilator-associated pneumonia could be a rapid alternative diagnostic method which permits the definite diagnosis of pneumonia. Accordingly, specific markers of VAP, namely the presence of intracellular microorganisms, the detection of elastin fibres, the antibody-coated bacteria test, the level of endotoxin in bronchoalveolar lavage fluid, the local production of interleukin-8, the levels of lactate dehydrogenase, and decreased surfactant protein A, may be important as they can provide a rapid diagnosis of VAP. Among the markers alluded to above, the search for intracellular bacteria in polymorphonuclear leukocytes or macrophages is the most widely validated technique with an excellent specificity, provided that prior antibiotics are not given. However, this technique has its own limitations; it requires a considerable time effort for the microbiologist, and also compels the performance of BAL, a technique not always harmless to the patient.
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PMID:Markers of ventilator-associated pneumonia. 1015 May 59

Group B streptococci (GBS) are the leading cause of pneumonia and sepsis in human newborns. Exudative pulmonary edema and alveolar hemorrhage seen in GBS pneumonia indicate vascular damage, and we reported that GBS injure lung microvascular endothelial cells (LMvEC) both in vivo and in vitro. The specific GBS factors causing LMvEC injury are uncertain, but GBS beta-hemolysin activity is associated with lung epithelial cell injury. We hypothesized that GBS beta-hemolysin contributes to LMvEC injury and exudative pulmonary edema. To test this hypothesis we used isogenic nonhemolytic and hyperhemolytic GBS mutants derived by transposon insertional mutagenesis from three different wild-type strains. Hemolytic titers for each strain were calculated using live GBS and Tween 80/starch-stabilized extracts of log-phase GBS. All nonhemolytic mutants lacked detectable hemolytic activity, whereas hyperhemolytic mutants produced 4-16 times the hemolytic activity of their parent strains. LMvEC injury was assayed by light microscopy, the release of lactate dehydrogenase, trypan blue nuclear staining and Evans blue-albumin flux. Compared with the parent strains, all nonhemolytic mutants caused significantly reduced, and all hyperhemolytic mutants caused significantly greater lactate dehydrogenase release from and trypan blue nuclear staining of LMvEC. Moreover, a nonhemolytic mutant caused reduced and a hyperhemolytic mutant caused increased Evans-blue albumin flux across polar LMvEC monolayers. These findings were corroborated by light microscopic evidence of hemolysin-associated damage to the LMvEC monolayers. We conclude that GBS beta-hemolysin promotes LMvEC injury and increases permeability in vitro, and speculate that GBS beta-hemolysin contributes to the pathogenesis of alveolar edema and hemorrhage in early onset GBS pneumonia.
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PMID:Group B streptococcal beta-hemolysin promotes injury of lung microvascular endothelial cells. 1023 55

The assessment of severity is one of the most important issues in the management of the patient with community-acquired pneumonia. If forms the basis of decisions about hospitalization or admission to an intensive care unit. Age, comorbid illness and vital sign abnormalities have been shown to represent the principal criteria of pneumonia severity. Severe community-acquired pneumonia is characterized by one or more of the following criteria: acute respiratory failure, haemodynamic compromise, severe sepsis and septic shock, multilobar radiographic infiltrates, plus some additional laboratory parameters (blood urea nitrogen > 7 mM, lactate dehydrogenase > 260 U.L-1 and low serum albumin at admission). Several sets of corresponding simple clinical and laboratory criteria have consistently been shown to have considerable potential in predicting death caused by pneumonia. It was recently found that the tentative definition of severe community-acquired pneumonia provided by the American Thoracic Society guidelines is highly sensitive but poorly specific. An alternative rule, defining severe pneumonia as the presence of two of three minor criteria (systolic blood pressure < 90 mmHg, multilobar involvement and arterial oxygen tension/inspiratory oxygen fraction < 250) or one of two major criteria (mechanical ventilation and septic shock), had a sensitivity of 78%, a specificity of 94%, a positive predictive value of 75% and a negative predictive value of 95%. When validated in an independent patient population, this rule may contribute to a more uniform definition of severe community-acquired pneumonia.
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PMID:Severe community-acquired pneumonia: how to assess illness severity. 1044 81

The aim of the study was to validate the prediction rule of M.J. Fine and coworkers for clinical outcome variables and three prognostic rules for the individual outcome of community-acquired pneumonia in an elderly population (rule 1: respiratory frequency > or =30 breaths x min(-1), diastolic blood pressure < or =60 mmHg, blood urea nitrogen >7 mM; rule 2: respiratory frequency > or =30 breaths x min(-1), diastolic blood pressure < or =60 mmHg, mental confusion; and rule 3: systolic blood pressure < or =80 mmHg, cardiac frequency > or =90 beats x min(-1), lactate dehydrogenase activity > or =260 IU x L(-1); death was predicted in the presence of at least two of three parameters). Overall 168 consecutive episodes of community-acquired pneumonia in patients aged > or =65 yrs and hospitalized in a primary care hospital were studied prospectively. Fine's rule was tested for its ability to predict length of hospital stay, requirement for intensive care unit (ICU) admission and death. For the three prognostic rules of individual outcome, performance regarding predicting death was determined. Mortality was 17/168 (10%). Fine's rule accurately predicted length of stay, the requirement for ICU admission and the risk of death from pneumonia as compared to the original derivation and validation cohorts. All three rules achieved moderate-to-high specificity (73%, 88% and 80%, respectively) and high negative predictive values (95%, 94% and 93%, respectively) but had a low sensitivity (65%, 47% and 47%, respectively). Rule 2 most closely reflected the risk of death from pneumonia when Fine's classification was used as reference. Fine's rule proved to give valid estimations regarding clinical outcome variables of community-acquired pneumonia in the elderly. The prognostic rules may be useful in determining individual patients at lower risk of death caused by pneumonia.
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PMID:Comparative validation of prognostic rules for community-acquired pneumonia in an elderly population. 1051 16

Determination of the cellular profile of bronchoalveolar lavage fluid (BALF), lactate dehydrogenase (LDH) and alkaline phosphatase (ALP) appeared to be useful in monitoring pulmonary damage. The aim of this study was to investigate whether the cellular profile, LDH, its isoenzyme pattern and/or ALP in BALF are useful in the diagnostic work-up of patients with suspected pneumonia. The BALF specimens of 80 patients were studied. Group I consisted of patients with a pulmonary infection (n=33) and group II of patients without signs of a pulmonary infection (n=47). Differentiation between these two groups was based upon the results of microscopy and quantitative cultures. The absolute as well as relative numbers of polymorphonuclear neutrophils (PMNs) was significantly higher in group I compared to group II (p<0.0001). The absolute number of PMNs showed a sensitivity of predicting the correct group of 95.7% and a specificity of 84.8%. The LDH activity in BALF was significantly higher in group I than in group II (p<0.0001). The LDH4/LDH5 ratio in BALF was lower in group I compared to group II (p<0.0001) and appeared to be the best discriminator between the two groups with a sensitivity of 93.6% and a specificity of 93.9%. In conclusion, the number of polymorphonuclear neutrophils as well as the lactate dehydrogenase activity, particularly its isoenzymes, in bronchoalveolar lavage fluid appeared to be of potential practical value to distinguish between infectious and noninfectious pulmonary disorders.
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PMID:Diagnostic value of BAL fluid cellular profile and enzymes in infectious pulmonary disorders. 1054 66

This review summarizes current strategies in the treatment of patients with pleural effusion. To determine whether a patient has a transudative or exudative pleural effusion, Light's criteria should be applied to measure the concentrations of protein and lactate dehydrogenase (LDH) in the pleural fluid and serum. If the effusion is transudative, therapy should be directed toward the underlying congestive heart failure, cirrhosis, or nephrosis. Consideration should be given to pleurodesis with a sclerosant if patients with recurrent transudative effusion have severe dyspnea due to their effusion. If the effusion is exudative, attempts should be made to define the etiology. The diagnosis of pleural malignancy is most easily established via pleural fluid cytology. If this is negative and the patient is suspected of having pleural malignancy, thoracoscopy is indicated. The concentrations of adenosine deaminase and gamma-interferon in pleural fluid are useful in the diagnosis of pleural tuberculosis. Patients with pneumonia and pleural effusion should undergo therapeutic thoracentesis; the pleural fluid should be Gram-stained and cultured, and the differential cell count, glucose and LDH concentration, and pH should be determined. Indicators of a poor prognosis include the presence of frank pus, a positive Gram-stain, a pleural glucose concentration of less than 2.2 mmol/L, a pH less than 7.00, the presence of pleural loculations, and an LDH concentration greater than three times the upper limit of normal in serum. If the pleural fluid cannot be completely evacuated because of loculations, intrapleural thrombolytic therapy should be considered. If thrombolytics are ineffective, thoracoscopy or thoracotomy with decortication should be performed. Dyspneic patients with malignant pleural effusions whose dyspnea is relieved with therapeutic thoracentesis should be considered for pleurodesis using a tetracycline derivative. Talc is not recommended because it induces acute respiratory distress syndrome in about 5% of patients, with an overall mortality of 1%.
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PMID:Management of pleural effusions. 1092 61


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